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Glycolytic reprogramming through PCK2 regulates tumor initiation of prostate cancer cells

  1. Author:
    Zhao, Jiangsha
    Li, Jieran
    Fan, Teresa W M
    Hou, Steven

  2. Author Address

    The Basic Research Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA., Graduate Center of Toxicology and Cancer Biology, Center for Environmental and Systems Biochemistry, and Markey Cancer Center, University of Kentucky, Lexington, KY 40536, USA.,
    1. Year: 2017
    2. Date: Oct 13
    3. Epub Date: 2017 Jun 28
  2. Journal: Oncotarget
    1. 8
    2. 48
    3. Pages: 83602-83618
  4. Type of Article: Article
  1. Abstract:

    Tumor-initiating cells (TICs) play important roles in tumor progression and metastasis. Identifying the factors regulating TICs may open new avenues in cancer therapy. Here, we show that TIC-enriched prostate cancer cell clones use more glucose and secrete more lactate than TIC-low clones. We determined that elevated levels of phosphoenolpyruvate carboxykinase isoform 2 (PCK2) are critical for the metabolic switch and the maintenance of TICs in prostate cancer. Information from prostate cancer patient databases revealed that higher PCK2 levels correlated with more aggressive tumors and lower survival rates. PCK2 knockdown resulted in low TIC numbers, increased cytosolic acetyl-CoA and cellular protein acetylation. Our data suggest PCK2 promotes tumor initiation by lowering acetyl-CoA level through reducing the mitochondrial tricarboxylic acid (TCA) cycle. Thus, PCK2 is a potential therapeutic target for aggressive prostate tumors.

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  1. Keywords:

External Sources

  1. View Full Text
  2. DOI: 10.18632/oncotarget.18787
  3. PMID: 29137367
  4. PMCID: PMC5663539
  5. View record in Web of Science®
  6. WOS: 000413030900019

Library Notes

  1. Fiscal Year: FY2016-2017
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